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* Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109;
Center for Immunology, Mount Sinai School of Medicine, New York, NY 10029; and
Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710
We have established a defect in CCR6–/– mice in response to a cockroach allergen airway challenge characterized by decreased IL-5 production, reduced CD4+ T and B cells as well as decreased eosinophil accumulation. To determine the nature of the defect in CCR6–/– mice T lymphocyte populations from allergen-sensitized wild-type mice were transferred into sensitized CCR6–/– mice. The reconstituted response was characterized by an increase in IL-5 levels, eosinophil accumulation, and serum IgE levels in recipient CCR6–/– mice. Analysis of lymphocytes from draining lymph nodes of CCR6+/+ and CCR6–/– sensitized or challenged mice demonstrated a significant decrease in IL-5 and IL-13 production in CCR6–/– mice. In contrast, the systemic response in allergen-rechallenged spleen cells demonstrated no significant alteration in allergen-induced cytokine production. Transfer of isolated splenic T lymphocytes from sensitized CCR6+/+ mice induced airway hyperresponsiveness in wild-type but not CCR6–/– naive mice, suggesting that T cells alone were not sufficient to induce airway hyperresponsiveness in CCR6–/– mice. Additional analysis demonstrated decreased CD11c+, CD11b+ and CD11c, and B220 subsets of dendritic cells in the lungs of CCR6–/– mice after allergen challenge. Using in vitro cell mixing studies with isolated pulmonary CD4+ T cells and CD11c+ cells from CCR6+/+ or CCR6–/– mice, we demonstrate alterations in both CCR6–/– T cells and CCR6–/– pulmonary APCs to elicit IL-5 responses. Altogether, the defect in CCR6–/– mice appears to be primarily due to an alteration in T cell activation, but also appears to include local pulmonary APC defects.
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